Slow wave sleep disruption increases cerebrospinal fluid amyloid-β levels
Yo-El S Ju1,2, Sharon J Ooms3,4,5, Courtney Sutphen1,2
1Department of Neurology, Washington University, Saint Louis, Missouri, USA.
Abstract:
See Mander et al. (doi:10.1093/awx174) for a scientific commentary on this article.Sleep deprivation increases amyloid-β, suggesting that chronically disrupted sleep may promote amyloid plaques and other downstream Alzheimer's disease pathologies including tauopathy or inflammation. To date, studies have not examined which aspect of sleep modulates amyloid-β or other Alzheimer's disease biomarkers. Seventeen healthy adults (age 35-65 years) without sleep disorders underwent 5-14 days of actigraphy, followed by slow wave activity disruption during polysomnogram, and cerebrospinal fluid collection the following morning for measurement of amyloid-β, tau, total protein, YKL-40, and hypocretin. Data were compared to an identical protocol, with a sham condition during polysomnogram. Specific disruption of slow wave activity correlated with an increase in amyloid-β40 (r = 0.610, P = 0.009). This effect was specific for slow wave activity, and not for sleep duration or efficiency. This effect was also specific to amyloid-β, and not total protein, tau, YKL-40, or hypocretin. Additionally, worse home sleep quality, as measured by sleep efficiency by actigraphy in the six nights preceding lumbar punctures, was associated with higher tau (r = 0.543, P = 0.045). Slow wave activity disruption increases amyloid-β levels acutely, and poorer sleep quality over several days increases tau. These effects are specific to neuronally-derived proteins, which suggests they are likely driven by changes in neuronal activity during disrupted sleep.
Insights
Disrupting slow wave sleep acutely raises amyloid-beta levels. Additionally, poor sleep quality over days is linked to increased tau, suggesting sleep impacts Alzheimer's disease biomarkers.
Area of Science:
- Neuroscience
- Sleep Medicine
- Biomarkers of Alzheimer's Disease
Background:
- Chronic sleep disruption is implicated in Alzheimer's disease (AD) pathologies, including amyloid-beta (Aβ) plaque formation.
- Previous research suggests a link between sleep deprivation and increased Aβ, but specific sleep aspects modulating AD biomarkers remain unclear.
Purpose of the Study:
- To investigate the impact of specific sleep disruptions on key Alzheimer's disease biomarkers.
- To determine whether acute disruption of slow-wave activity or chronic poor sleep quality affects Aβ and tau levels.
Main Methods:
- Seventeen healthy adults (35-65 years) underwent actigraphy for sleep monitoring.
- Polysomnography was used to disrupt slow-wave activity, followed by cerebrospinal fluid collection.
- Cerebrospinal fluid biomarkers including Aβ40, tau, and YKL-40 were measured and compared to a sham condition.
Main Results:
- Acute disruption of slow-wave activity specifically increased amyloid-beta40 levels (r = 0.610, P = 0.009).
- This effect was independent of sleep duration or efficiency and did not affect other measured proteins.
- Poorer overnight sleep efficiency over several days was associated with higher tau levels (r = 0.543, P = 0.045).
Conclusions:
- Acute slow-wave activity disruption elevates amyloid-beta levels, suggesting a direct impact on Aβ metabolism.
- Chronic poor sleep quality, indicated by reduced sleep efficiency, is linked to increased tau.
- These findings highlight the specific roles of different sleep characteristics in modulating neuronal protein biomarkers relevant to Alzheimer's disease.
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